Focal segmental glomerulosclerosis (FSGS) is a kidney tissue-lesion disease where glomerular sclerosis occurs the kidney. The clinical manifestation of which are nephrotic syndromes, comprising severe proteinuria, hypertension, hypoalbuminemia and hematuria etc. (Cattran D C, Rao P. American Journal of Kidney Disease, 21(3):344-9, 1998; Chun M J et al., Journal of the American Society of Nephrology, 15:2169, 2004; Rydel J J et al., American Journal of Kidney Disease, 25(4):534-42, 1995). During the initial phase of the disease, the symptoms include thickening of the glomerular basement membrane, increasing of glomerular extracellular matrix, appearance of deposition of hyaline masses in blood vessels, and finally the formation of scar tissues composed mainly of collagen, accompanied by accumulation of foam cells on the capillary wall, capillary collapse, hyperplasia and hypertrophy of visceral epithelial cells, and podocyte fusion; the sclerotic portion expands gradually with the progression of the disease (D'Agati V D. Curr Opin Nephrol Hypertens 17(3):271-81, 2008; Hodgin J B et al., American Journal of Clinical Pathology, 177(4):1674-86, 2010; and Thomas D B., The Archives of Pathology and Laboratory Medicine. 133(2):217-23, 2009). Podocytes mainly distribute on the glomerular basement membrane, their function being the filtration of blood. Super resolution microscopy is currently able to observe the damaged condition of the podocytes in the glomerulus of a FSGS patient, which is considered as one of the main reasons of the sclerosis of the glomerulus (Kriz W et al., Kidney International. 54(3):687-97, 1998. Pagtalunan M E et al. The Journal of Clinical Investigation. 99(2):342-8, 1997. Wiggins J E et al. Journal of the American Society of Nephrology. 16(10):2953-66, 2005. Yang H C et al., Kidney International. 69(10):1756-64, 2006).
The number of focal segmental glomerulosclerosis (FSGS) patients increase each year in various countries. However, its pathological mechanism is not yet fully understood. Possible causes are other types of nephritis, such as focal proliferative nephritis, vasculitis, lupus nephritis, kidney transplant, or toxic damage (Bahiense-Oliveira M et al. Clinical Nephrology. 61:90-7, 2004. D'Agati V. Seminars in Nephrology. 23:117, 2003). Clinically, it is treated by cytotoxic drugs (e.g. cyclophosphamide), immunosuppressants (e.g. cyclosporine, Mycophenolate Mofetil), non-steroidal anti-inflammatory drugs (NSAIDs), vasodilators, or solely by corticosteroids (e.g. prednisolone). However, only 20%-40% of the patients are responsive to treatment by steroids, and it is only effective after long-term administration. Even after the treatment by steroids, there is still a chance for the disease to develop to an end-stage renal disease in a patient (Beba N et al., Turkish Journal of Pediatric. 52(3):255-61, 2010. Daskalakis N, Winn M P. Cellular and Molecular Life Sciences. 63(21):2506-11, 2006. Gipson D S et al., Kidney International. 80 (8):868-78, 2011. Daskalakis N, Winn M P. Cellular and Molecular Life Sciences. 63(21):2506-11, 2006. Gipson D S et al., Kidney International. 80 (8):868-78, 2011. Kanjanabuch T et al, Journal of The Medical Association of Thailand. 2:S262-79, 2006). In addition, these drugs often produce harmful side-effects, such as drug resistance and renal toxicity, which generates greater harm to the human body, and there are also issues such as recurring after discontinuance of use of the drug.
Osthole, its nomenclature being 7-methoxy-8-(3-methylbut-2-enyl)-2-chromanone, and its molecular formula being C15H16O3, has the following structure:

Osthole can be extracted from the seeds of the Apiaceae genus plant Cnidium monnieri, which is already known to possess anti-microbial-infection, anti-proliferation and anti-allergic effects. However, no prior art has disclosed its renal protective effects of osthole in treating or relieving various symptoms of focal segmental glomerulosclerosis.